Interpretive Summary: Acquisition of the element phosphorus (P) from soil is a major factor limiting crop productivity and quality. Although large amounts of fertilizer P are applied on farms each year, only about 20% is used by the crop and the remainder is bound to soil. In addition, in many parts of the world P fertilizer is too costly to apply and the amount of P in soils is quite low. It is crucial that we understand how plants acquire P and how t improve the efficiency of P uptake by crops. White lupin plants have several adaptative features to increase the efficiency of P acquisition. Among these adaptations are changes in root structure and chemistry. In this study we evaluated factors that control changes in white lupin root development in response to inadequate P. Our results show that plant growth hormones produced in shoots of P-stressed plants are critical to modifying root development. Treatments that block the transport of growth hormones from the shoot to the root block the changes induced in root growth due to low P. In addition, blocking of growth hormone transport from shoot to root also blocked the chemical changes in roots of P-stressed plants. Results from this study are important because they identify plant growth hormones as critical for white lupin adaptation to low P stress. These findings give crop scientists several novel approaches toward improving the acquisition of P by plants.

Technical Abstract:
White lupin (Lupinus albus L.) develops proteoid (cluster) roots in response to phosphorus deficiency. Auxins are required for lateral root development, but little is known of their role in proteoid root formation. Proteoid root numbers were dramatically increased in P-sufficient (+P) plants by application of the synthetic auxin napthalene acetic acid (NAA) to leaves and were reduced in P-deficient (-P) plants by the presence of auxin transport inhibitors [2,3,5-triiodobenzoic acid (TIBA) and naphthylaphthalamic acid (NPA)]. Although ethylene concentrations in the root zone were 1.5 fold higher in -P plants, there was no effect on proteoid root numbers of the ethylene inhibitors aminovinvylglycine (AVG) and silver sulfate (AgSO4). Phosphonate, which interferes with plant perception of internal P concentration, dramatically increased the number of proteoid root segments in +P plants. Activities of PEPC, MDH, and exuded dacid phosphatase in proteoid root segments were not different from +P controls when NAA was applied to +P lupin plants, but increased to levels comparable to -P plants in the phosphonate treatment. Addition of TIBA or NPA to -P plants reduced PEPC and MDH activity of -P proteoid roots to levels found in +P or -P normal root tissues, but did not affect acid phosphatase in root exudates. These results suggest that auxin transport from the shoot plays a role in the formation of proteoid roots during P deficiency. Auxin-stimulated proteoid root formation is necessary, but not sufficient, to signal the up-regulation of PEPC and MDH in proteoid root segments. In contrast, phosphonate applied to P-sufficient white lupin elicits the full suite of coordinated responses to P deficiency.